Protective effects of alpha-lipoic Acid on oleic Acid-induced acute lung injury in rats.

BACKGROUND: Oxidative stress is believed to be an important factor in the pathogenesis of acute lung injury (ALI). AIMS: The aim of this study was to investigate the possible protective role of alpha-lipoic acid (α-LA) on oleic acid (OA)-induced ALI in rats. STUDY DESIGN: Animal experiment. METHODS: A total of thirty-five rats were divided into five groups in the study. Group 1 served as a control group. Rats in Group 2 (α-LA) were administered α-LA intraperitoneally at a dose of 100 mg/kg body weight (BW). Rats in Group 3 (OA) were administered OA intravenously at a dose of 100 mg/kg BW. In Group 4 (pre-OA-α-LA), α-LA was given 15 minutes prior to OA infusion, and in Group 5 (post-OA-α-LA), α-LA was given two hours after OA infusion. Four hours after the OA infusion, rats were decapitated. Blood samples were collected to measure serum levels of malondialdehyde (MDA) and glutathione (GSH), and the levels of activity for superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px). Lung tissue samples were taken for histopathological examination. RESULTS: Exposure to OA resulted in increases in serum MDA levels (p<0.001), as well as histopathological lesions in lung tissue, and decreases in CAT (p<0.05), GSH-Px (p<0.05) activities and GSH (p<0.05) levels. On the other hand, MDA levels were decreased significantly (p<0.001), while CAT (p<0.05), GSH-Px (p<0.01) activities and GSH (p<0.05) levels were increased significantly in the pre-OA-α-LA group compared with the OA group. CONCLUSION: α-LA was found to lessen oxidative stress and to have positive effects on antioxidants in cases of OA-induced ALI. In conclusion, α-LA appears to have protective effects against ALI and potential for the prevention of ALI.

Effects of lycopene on the model of oleic acid-induced acute lung injury.

INTRODUCTION: This study, we aimed to investigate the protective effect of lycopene in lung injury rat model. MATERIALS AND METHODS: Twenty eight Wistar rats were enrolled into the study. Control group (n= 7) were applied PBS + ethanol (9/1). A single dose of 100 mg/kg oleic acid (OA) intravenously was administrated to OA group (n= 7). One mL of corn oil was given daily to corn oil + OA group (n= 7) by gavage for five weeks. Lycopene was given by gavage to lycopene + OA group (n= 7) for five weeks. At the end of the 5th weeks, OA were given. Four hour after OA administration, lung tissue, blood samples were taken. Malondialdehyde, superoxide dismutase, glutathione-peroxidase, catalase levels were determined. RESULTS: Malondialdehyde levels of serum, lung tissues were increased in OA, corn oil + OA groups than control, where as decreased to controls levels in lycopene + OA group (p< 0.05). Superoxide dismutase, glutathione-peroxidase activities of serum, tissue increased moderetaly or they were closed with control values. There was significant increase in lycopene + OA group values. Histopathological examination of control group was normal. OA, cornoil + OA groups had perivascular, alveolar edema, hemorrage, prominent neutrophil infiltration, destruction in alveolar structure. Lycopene + OA group had less neutrophilic infiltration, perivascular, alveolar edema. CONCLUSION: Lycopene rich diet may have an important role preventing damages in lungs.

[Serum ghrelin, IL-6 and TNF-α levels in patients with chronic obstructive pulmonary disease.]. / Kronik obstrüktif akciger hastaligi olan olgularda serum grelin, IL-6 ve TNF-α düzeyleri.

It is determined that endocrine factors can play role on cachexia in chronic obstructive pulmonary disease (COPD). High levels of ghrelin is reported in cachectic COPD cases but its' relation couldn't shown statistically. In our study, it is aimed to detect serum ghrelin levels in COPD, its' relation with proinflammatory cytokines and whether serum ghrelin is associated with cachexia. Sixty stable COPD patients and 15 healthy volunteers were included in the study. COPD patients were divided into two groups, cachectic and normal weight, according to their body mass index. Spirometric assessments were performed and serum tumor necrosis factor-alpha (TNF-a), interleukin-6 (IL-6) and ghrelin levels were measured in all cases. When COPD patients were compared with control group; serum ghrelin levels were statistically lower, TNF-a and IL-6 levels were statistically higher in COPD group. For cachectic COPD patients; serum ghrelin levels were statistically lower and IL-6 levels were statistically higher, compared with normal weight COPD patients. Although, serum TNF-a levels were higher for cachectic COPD patients; these levels were not significant. Positive correlation between serum ghrelin levels and body mass index was detected in patients with COPD. As a result; it is thought that increased proinflammatory cytokines and decreased serum active ghrelin levels may contribute to the development of weight loss.

[Effects of erdosteine on inflammation and fibrosis in rats with pulmonary fibrosis induced by bleomycin]. / Ratlarda bleomisin ile olusturulan akciger fibrozisinde erdosteinin inflamasyon ve fibrozis üzerine etkileri.

We aimed to investigate the levels of some chemokines, inflammatory cell counts in bronchoalveolar lavage (BAL) fluid, histopathological changes in lung tissue, to determine the effect of erdosteine on acute inflammatory changes and fibrosis in a rat fibrosis model induced by bleomycine (BLM). Forty-five Wistar male rats were taken into the study. On day 0, intratracheal saline to control group (group 1, n= 15), intratracheal BLM 7.5 U/kg to BLM (group 2, n= 15) and erdosteine group (group 3, n= 15) was administered. In group 3, oral erdosteine (10 mg/kg/day) was applied two days before BLM. On day 0, 14, and 29th five rats in each groups were sacrificed, BAL fluid was performed. Malonyldialdehyde (MDA), macrophage inflammatory protein (MIP)-1alpha, MIP-2 levels in BAL fluid, hydroxyproline levels in lung tissue were measured. Histopathological examination was performed. When BLM group compared to erdosteine group, the levels of MDA, MIP-1alpha, MIP-2, and neutrophil counts, the hydroxyproline (OH-P) level of lung tissue were decreased in erdosteine group on acute inflammatory phase (day 14) (p< 0.001, p= 0.017, p= 0.009, p< 0.001, p= 0.009, respectively), and late fibrosis phase (day 29) except BAL MIP-2 (p= 0.022, p= 0.025, p= 0.01, p< 0.001, respectively). Fibrosis level was significantly lower in erdosteine group than BLM group on day 29 (p= 0.01). We conclude that erdosteine may prevent the acute lung inflammation and fibrosis by suppressing the accumulation of neutrophils, inhibition of lipid peroxydation, chemokine production, and release.

The evaluation of cognitive functions with P300 test for chronic obstructive pulmonary disease patients in attack and stable period.

OBJECTIVES: Hypoxia, in chronic obstructive pulmonary disease (COPD), leads to a decrease in cerebral perfusion and an impairment of some cognitive abilities. We aimed to investigate the relation between arterial blood gas analysis (ABA) and pulmonary function test (PFT) parameters with cognitive function of COPD patients during attack and stable period. PATIENTS AND METHODS: ABA, PFT, P300 tests of 30 patients in stabilized period and 30 patients in attack, and 17 healthy controls were evaluated. RESULTS: When both COPD groups and controls were compared, it was seen that latency of P300 was shorter in the control group (p<0.001), but there was no difference between COPD groups (p>0.05). P300 amplitude measures were lower in both COPD groups than control group, but it was not statistically significant (p>0.05). When we compared the measures of attack group, we saw that arterial oxygen tension (PaO(2)), arterial oxygen saturation (SaO(2)), forced expiratory volume in 1s (FEV(1)), FEV(1)/forced vital capacity (FVC) values increased (p<0.001), and P300 latency shortened (p<0.05) in attack group during stable period. P300 latency correlated significantly with PaO(2) (r=-0.557, p<0.001), SaO(2) (r=-0.424, p<0.001), FEV(1) (r=-0.441, p<0.001), FEV(1)/FVC (r=-0.477, p<0.001) values, and age (r=0.329, p<0.05). P300 amplitude is only correlated with PaO(2) (r=0.236, p<0.05). CONCLUSION: Longer latency of P300 appears to be an expected sequel of COPD. P300 test can be considered as a potential objective marker of cognitive impairment.